Management of Viral Hepatitis in Immunocompromised Patients

Mohammed A. SuwaidMohammed A. Suwaid
Egyptian Fellowship Board CandidateEgyptian Fellowship Board Candidate
Medical OncologyMedical Oncology
June 2014June 2014
Management of Viral Hepatitis inManagement of Viral Hepatitis in
Immunocompromised PatientsImmunocompromised Patients

The Agenda
 Overview of viral hepatitis.
 Definition of the immunocompromised host.
 The relationship between immunosuppression and hepatitis.
 Management approach.

Definition and Etiology of Hepatitis
 Hepatitis is an inflammation of the liver characterized by diffuse or patchy
necrosis.
 Common causes include:
• Specific hepatitis viruses (A, B, C, D and E)
• Alcohol
• Drugs (eg, INH)

Definition and Etiology of Hepatitis
 Less common causes include:
• Other viral infections (eg, IMN, yellow fever and CMV)
• Parasitic infections (eg, schistosomiasis, malaria and amebiasis)
• Leptospirosis
• Autoimmune diseases
• Metabolic diseases

Viral Hepatitis
 Viral hepatitis accounts for more than 50% of cases of acute hepatitis in the
United States.
 HAV, HBV, and HCV are the most common types of viral hepatitis.
 These can result in acute disease (subclinical disease, self-limited
symptomatic disease or FHF).
 Most cases of acute viral hepatitis resolve spontaneously.

Viral Hepatitis
 Acute hepatitis A or B are usually symptomatic (nausea, abdominal pain,
fatigue, malaise, and jaundice).
 Most cases of acute hepatitis C are asymptomatic.
 HBV and HCV can lead to chronic infection with subsequent cirrhosis and
hepatocellular carcinoma (HCC).
 Chronic carriers may transmit the disease for many years.

Viral Hepatitis
 Severe cases of acute hepatitis may progress rapidly to acute liver failure.
 This is marked by poor hepatic synthetic function (defined as a PT of 16
seconds or an INR of 1.5 in the absence of previous liver disease).
 If acute liver failure is complicated by hepatic encephalopathy then it is
called FHF.

Viral Hepatitis
 The encephalopathy of FHF is attributed to:
• increased permeability of the BBB.
• impaired osmoregulation in the brain, which leads to brain-cell swelling.
 The resulting brain edema is a potentially fatal.

Types of Viral Hepatitis
at a Glance

Case # 01: A 45-year-old farmer presented to you complaining of easy fatigability, nausea,
and abdominal pain for the past 3 days. He is a known case of Hodgkin’s lymphoma on
chemotherapy (doxorubicin, bleomycin, vinblastine and dacarbazine on days 1+14 every 4
weeks) started 2 months ago with good response (disappearance of his cervical LAP). On
examination, there is mild jaundice, pallor, grade I oral mucositis, tenderness on the right
hypochondrial region without hepatomegaly, splenomegaly nor palpable lymphadenopathy.
U/S of the abdomen was normal. Laboratory tests show the following:
What is the most likely diagnosis:
A. Hepatitis A B. Hepatitis B C. Hepatitis C
D. Hepatitis D E. Hepatitis E
Hb: 9.7 g/dL (12-17) ALT: 245 U/L (10-55) Anti-HAV IgG: positive
TLC: 3.5 × 103
/uL (4-10.5 × 103
) AST: 220 U/L (10-40) HBsAg: negative
Plt: 110 × 103
/uL (150-450 × 103
) ALP: 130 U/L (45-115) Anti-HCV: positive
MCV: 80 fL (79-97) Total bilirubin: 1.7 mg/dL (<1) HCV RNA: negative
BUN: 35 mg/dL (15-40) Albumin: 4.1 g/dL (3.1-4.3) Anti-HIV: negative
Serum Creatinine: 1.0 mg/dL (<1.2) INR: 1

Hepatitis A Virus (HAV)
 A single-stranded RNA picornavirus.
 The most common cause of acute viral hepatitis (>75% of adults ).
 Particularly common among children and young adults.
 It spreads primarily by fecal-oral contact.
 Waterborne and food-borne epidemics.
 Sporadic cases are also common.
 HAV has no chronic carrier state.

 Diagnosis:
• Thorough history and physical examination.
• Anti-HAV IgM: acute infection.
• Anti-HAV IgG: previous infection (immunity).
 Treatment:
• Supportive.
• Contacts should be vaccinated.
• OCCPs and HRT should be stopped (risk of cholestasis).
• Alcohol consumption is not advised.
• Identify the patients with a risk of developing FHF (age >40 and those with CLD).

 Prevention:
• By vaccination.
• Preexposure prophylaxis provides long-term protection (20 years).
• Postexposure prophylaxis should be given as early as possible.

Hepatitis B Virus (HBV)
 The most complex hepatitis virus.
 Consists of a viral core plus an outer surface coat.
 The core contains circular double-stranded DNA and DNA polymerase.
 Replicates within the nuclei of infected hepatocytes.
 It is the 2nd
most common cause of acute viral hepatitis.
 Parenterally transmitted.
• patients in renal dialysis units
• patients in oncology units
• hospital personnel in contact with blood

Hepatitis B Virus (HBV)
 May spread through contact with other body fluids (eg, between sex
partners).
 Vertical transmission from mother to infant is common.
 Sporadic cases can also occur.
 Serologic diagnosis: HBsAg.

Hepatitis C Virus (HCV)
 A single-stranded RNA flavivirus.
 Six major HCV genotypes.
 These subtypes vary in geographic distribution, virulence and response to
therapy.
 HCV can produce quasispecies.
 Parenterally transmitted.

Hepatitis C Virus (HCV)
 Sexual transmission and vertical transmission are relatively rare.
 Sporadic cases can occur.
 Serologic diagnosis: Anti-HCV.

Hepatitis D Virus (HDV)
 Delta agent.
 Defective RNA virus that can replicate only in the presence of HBV.
 It occurs as a coinfection or a superinfection with HBV infection.
 Infected hepatocytes contain delta particles coated with HBsAg.
 Parenteral drug users are at a relatively high risk.
 Serologic diagnosis: Anti-HDV.
 Treatment: No specific treatment is available. Some success has been
reported with foscarnet.
 Prevention: by prevention of hepatitis B.

Hepatitis E Virus (HEV)
 RNA virus.
 Enterically transmitted.
 Waterborne outbreaks due to fecal contamination of the water supply, have
occurred in northern Africa and other countries.
 Sporadic cases can occur.
 HEV was not originally thought to cause chronic hepatitis, cirrhosis or
chronic carrier state except in immunocompromised patients.

Hepatitis E Virus (HEV)
 Pregnant women are a special risk category (15% risk of FHF and 25%
mortality in the 3rd
trimester).
 Serologic diagnosis: Anti-HEV.
 Treatment: supportive.
 Prevention: avoid untreated drinking water, eating ice of unknown purity or
uncooked shellfish.
 There is no commercially available vaccine for HEV.

Characteristics of Hepatitis Viruses
Characteristic Hepatitis A Virus Hepatitis B Virus Hepatitis C Virus Hepatitis D Virus Hepatitis E Virus
Nucleic acid RNA DNA RNA * RNA
Serologic diagnosis IgM anti-HA HBsAg Anti-HCV Anti-HDV Anti-HEV
Major transmission Fecal-oral Blood Blood Needle Water
Incubation period
(days)
15–45 40–180 20–120 30–180 14–60
Epidemics Yes No No No Yes
Chronicity No Yes Yes Yes No
Liver cancer No Yes Yes Yes No
*Incomplete RNA; requires presence of hepatitis B virus for replication.
anti-HCV = antibody to hepatitis C virus; anti-HDV = antibody to hepatitis D virus; anti-HEV = antibody to hepatitis E virus; HBsAg = hepatitis B surface
antigen; IgM anti-HAV = IgM antibody to hepatitis A virus.

Case # 01: A 45-year-old farmer presented to you complaining of easy fatigability, nausea,
and abdominal pain for the past 3 days. He is a known case of Hodgkin’s lymphoma on
chemotherapy (doxorubicin, bleomycin, vinblastine and dacarbazine on days 1+14 every 4
weeks) started 2 months ago with good response (disappearance of his cervical LAP). On
examination, there is mild jaundice, pallor, grade I oral mucositis, tenderness on the right
hypochondrial region without hepatomegaly, splenomegaly nor palpable lymphadenopathy.
U/S of the abdomen was normal. Laboratory tests show the following:
What is the most likely diagnosis:
A. Hepatitis AA. Hepatitis A B. Hepatitis BB. Hepatitis B C. Hepatitis CC. Hepatitis C
D. Hepatitis DD. Hepatitis D E. Hepatitis EE. Hepatitis E
Hb: 9.7 g/dL (12-17) ALT: 245 U/L (10-55) Anti-HAV IgG: positive
TLC: 3.5 × 103
/uL (4-10.5 × 103
) AST: 220 U/L (10-40) HBsAg: negative
Plt: 110 × 103
/uL (150-450 × 103
) ALP: 130 U/L (45-115) Anti-HCV: positive
MCV: 80 fL (79-97) Total bilirubin: 1.7 mg/dL (<1) HCV RNA: negative
BUN: 35 mg/dL (15-40) Albumin: 4.1 g/dL (3.1-4.3) Anti-HIV: negative
Serum Creatinine: 1.0 mg/dL (<1.2) INR: 1

Management Approach ofManagement Approach of
Viral Hepatitis B and C inViral Hepatitis B and C in
Immunocompetent PatientsImmunocompetent Patients

 Case # 2: A 57-year-old male is presented to your clinic complaining of fatigue,
generalized muscle and joint pains and discomfort in the abdomen on the right side for 1
week. The patient has type II diabetes mellitus diagnosed 8 years ago on metformin and
glibenclamide. He has a history of brain surgery for removal of a tumor (glioblastoma) 3
months ago, received radiotherapy and now he is on oral temozolomide.
On examination, he is pale, slightly jaundiced, the abdomen is soft with right upper
quadrant tenderness.
You requested imaging and laboratory investigations and you confirmed the diagnosis of
acute hepatitis B.
what is the best treatment option in this situation:
A.IFN-ɑ
B.IFN- plus ribavirinɑ
C.Lamivudine
D.Tenofovir
E.Supportive

Acute Hepatitis BAcute Hepatitis B

 Diagnosis:
• Thorough history and physical examination.
• Principal symptoms:
• Fatigue and tiredness
• Malaise
• Jaundice
• Fever
• Muscle and joint aches
• Less common symptoms:
• Weight loss
• Depression
• Anxiety, irritability
• Headaches
• Sleep disturbance
• Discomfort in the abdomen on the
right side
• Itching
• Nausea and diarrhea
• Appetite loss

 Diagnosis:
• Serology:
• HBsAg: Positive.
• This will cleared within 6 months after the acute onset.
• A follow-up re-check this is essential in all cases.

 Treatment:
• Spontaneous recovery occurs in 95–99% of previously healthy adults.
• Antiviral therapy is, therefore, not required except in:
1. nonhepatic complication such as periarteritis nodosa.
2. immunocompromised individuals.
In these cases, antiviral therapy with lamivudine may be recommended.
• Intensive care may improve the survival in fulminant hepatitis.
• Full recovery with development of anti-HBs provides long-term protection.

Chronic Hepatitis BChronic Hepatitis B

 Presence of positive HBsAg >6 months.
 Initial evaluation:
• History and physical examination.
• Family history of liver disease and HCC.
• Laboratory tests: CBC, hepatic panel, and PT.
• HBsAg.
• Tests for HBV replication: HBeAg/anti-HBe, HBV DNA.

Initial evaluation:
• Tests to rule out viral coinfections: anti-HCV, anti-HDV and anti-HIV in those at risk.
• Tests to screen for HCC: AFP at baseline and ultrasound in high risk patients.
• Liver biopsy may be done to assess the degree of liver damage and to rule out other
causes of liver disease.
• Hepatitis A vaccination in those not immune to hepatitis A virus. Two doses, 6 to 18
months apart.

 Indications of treatment:
1. HBeAg-positive:
• if ALT >2 times normal OR moderate/severe hepatitis on biopsy, AND HBV
DNA >20,000 IU/mL.
• ALT normal or <2 times ULN if there is moderate or severe necroinflammation or
significant fibrosis on liver biopsy.
1. HBeAg-negative:
• HBV DNA >20,000 IU/mL AND elevated ALT >2 times normal.
Treatment may be initiated with any of the 7 approved antiviral medications but
pegIFN- , tenofovir or entecavirɑ are preferred.

 Indications of treatment:
3. Patients with compensated cirrhosis:
• ALT >2 times normal, OR HBV DNA levels >2,000 IU/mL.
They are best treated with nucleoside analogues (eg, tenofovir and entecavir)
because of the risk of hepatic decompensation associated with IFN- –relatedɑ
flares of hepatitis.
4. Patients with decompensated cirrhosis:
• Treatment should be promptly initiated with a nucleoside analogue that can
produce rapid viral suppression with low risk of drug resistance (Lamivudine or
telbivudine may be used as initial treatment in combination with adefovir or
tenofovir).

 Duration of treatment:
1. HBeAg-positive chronic hepatitis B:
• until the patient has achieved HBeAg seroconversion and
• undetectable serum HBV DNA and
• completed at least 6 months of additional treatment after appearance of anti-HBe.
1. HBeAg-negative chronic hepatitis B:
• until the patient has achieved HBsAg clearance.

 Duration of treatment:
3. Compensated cirrhosis: should receive long-term treatment.
• in HBeAg-positive patients: treatment may be stopped if they have confirmed
HBeAg seroconversion and have completed at least 6 months of consolidation
therapy.
• in HBeAg-negative patients: if they have confirmed HBsAg clearance.
• close monitoring for relapse is needed after withdrawal of treatment.
3. Decompensated cirrhosis and recurrent hepatitis B post–liver transplantation:
Life-long treatment is recommended.

Suggested follow-up:

Hepatitis BHepatitis B
 Prevention:
• Preexposure vaccination: effective in 95% of children and 90% of adults.
• Revaccination is effective in 80% of those who do not respond to the primary
vaccination.
• Postexposure prophylaxis: A combination of HBIg, when available, and HBV vaccine
is recommended.
• It is important to vaccinate within 24 hours.
• If HBIg is available (in most countries it is not), it should be given to all children of
HBsAg-positive mothers at the time of delivery.
• There is no evidence of a protective effect if the vaccine is given more than 7 days
after delivery.

Hepatitis BHepatitis B
 Prevention:
• Direct exposure (percutaneous inoculation or transmucosal exposure) to HBsAg
positive body fluid (eg, needlestick injury):
• HBIg single intramuscular dose of 0.06 mL/kg (as soon as possible).
• Followed by a complete course of HBV vaccination (initiated within 7 days).
• Direct exposure following sexual contact with an individual with HBV:
• HBIg single intramuscular dose of 0.06 mL/kg (within 14 days).
• Accompanied by a complete course of HBV vaccination as soon as possible.

 Case # 2: A 57-year-old male is presented to your clinic complaining of fatigue,
generalized muscle and joint pains and discomfort in the abdomen on the right side for 1
week. The patient has type II diabetes mellitus diagnosed 8 years ago on metformin and
glibenclamide. He has a history of brain surgery for removal of a tumor (glioblastoma) 3
months ago, received radiotherapy and now he is on oral temozolomide.
On examination, he is pale, slightly jaundiced, the abdomen is soft with right upper
quadrant tenderness.
You requested imaging and laboratory investigations and you confirmed the diagnosis of
acute hepatitis B.
what is the best treatment option in this situation:
A.A.IFN-ɑIFN-ɑ
B.B.IFN- plus ribavirinɑIFN- plus ribavirinɑ
C.C.LamivudineLamivudine
D.D.TenofovirTenofovir
E.E.SupportiveSupportive

Acute Hepatitis CAcute Hepatitis C

Diagnosis:
• History and physical examination.
• Laboratory tests: CBC, hepatic panel, and PT.
• anti-HCV (by ELISA):
• Positive in 50–70% of cases when symptoms begin.
• Positive in >90% after 3 months.
• It should be confirmed by RIA (recombinant immunoblot assay).

Diagnosis:
• HCV RNA (by PCR) is positive within 1–2 weeks after exposure. It is indicated in:
• Patients with a positive anti-HCV test.
• Patients for whom antiviral treatment is being considered, using a quantitative
assay.
• Patients with unexplained liver disease whose anti-HCV test is negative and who
are immunocompromised or suspected of having acute HCV infection.
• HCVcoreAg: can detect HCV infection about 1.5 months earlier than the anti-HCV
tests and an average of only 2 days later than quantitative HCV RNA detection.

 Treatment:
• Early identification and intervention can markedly reduce the risk of chronic infection
from 80% to 10%.
• Treatment is indicated in:
• HCV RNA–positive or
• HCVcoreAg positive
• Treatment consists of interferon-based anti-viral therapy for at least 12 weeks.
• No recommendation can be made for or against the addition of ribavirin and the
decision will therefore need to be considered on a case-by-case basis.
• Treatment can be delayed for 8 to 12 weeks after acute onset of hepatitis to allow for
spontaneous resolution.

 Prevention:
• There is no preexposure prophylaxis for HCV.
• Behavioral changes and limiting exposure to high risk situations offers the best
chance of primary prevention.
• Both therapeutic and prophylactic vaccines are currently under development.

Chronic Hepatitis CChronic Hepatitis C

 Presence of detectable viral replication for at least six months.
 Initial evaluation:
• HCV genotype should be determined prior to interferon-based treatment to:
1. Plan for the dose and duration of therapy.
2. Estimate the likelihood of response.
• Liver biopsy may be considered:
1. If the physician needs more information regarding fibrosis stage for prognostic purposes.
2. To make a decision regarding treatment.

 Treatment decisions should be individualized based on:
1. The severity of liver disease.
2. The potential for serious side effects.
3. The likelihood of treatment response.
4. The presence of comorbid conditions.
5. The patient’s readiness for treatment.

 Treatment is indicated in:
• Those with bridging fibrosis on biopsy.
• Compensated cirrhosis provided they do not have contraindications to therapy.
 The optimal therapy is the combination of pegIFN- and ribavirinɑ .
 HCV RNA should be tested by a highly sensitive quantitative assay at the
initiation of or shortly before treatment and at week 12 of therapy.

 Contraindications to treatment of chronic hepatitis C:
1. Major uncontrolled depressive illness.
2. Solid organ transplant (renal, heart, or lung).
3. Autoimmune hepatitis or other autoimmune condition known to be exacerbated by
peginterferon and ribavirin.
4. Untreated thyroid disease.
5. Pregnant or unwilling to comply with adequate contraception.
6. Severe concurrent medical disease.
7. Age less than 2 years.
8. Known hypersensitivity to drugs used to treat HCV.

 Treatment of genotypes 1 and 4 HCV infection:
• peginterferon plus ribavirin: for 48 weeks.
• Treatment may be discontinued in patients who do not achieve a partial EVR*.
• Patients who do not achieve a complete EVR♠
, should be re-tested at week 24, and if
HCV RNA remains positive, treatment should be discontinued.
* Partial EVR (partial early virological response): ≥2 log reduction in HCV RNA at week 12 of treatment.
♠ Complete EVR (complete early virological response): HCV RNA cannot be detected in the blood at week 12 of treatment.

 Treatment of genotypes 1 and 4 HCV infection:
• For patients with genotype 1 infection who have delayed virus clearance*, extend
therapy to 72 weeks.
• At the end of treatment, HCV RNA should be tested with a highly sensitive assay and
if the result is negative, it should be retested 24 weeks later to evaluate for a SVR♠
.
 Treatment of genotype 2 and 3 HCV Infection:
• peginterferon plus ribavirin: for 24 weeks, using a lower ribavirin dose.
• At the end of treatment, HCV RNA should be tested with a highly sensitive assay and
if the result is negative, it should be retested 24 weeks later to evaluate for a SVR.
* Delayed virus clearance: HCV RNA test becomes negative between weeks 12 and 24.
♠ SVR (sustained virological response): HCV RNA negative 24 weeks after cessation of treatment.

 Patients with HCV-related cirrhosis who achieve an SVR, regardless of the
genotype, should continue to be monitored at 6 to 12 month intervals for the
development of HCC.

 An immunocompromised host is a patient who does not have the ability
to respond normally to an infection due to an impaired or weakened
immune system. This inability to fight infection can be caused by a
number of conditions including:
• Primary immune deficiency.
• AIDS.
• Trauma.
• Diabetes mellitus.
• Malnutrition.
• Secondary to medical treatment such as chemotherapy or following organ
transplantation or HSCT.
http://emedicine.medscape.com/article/973120-overview
Immunocompromised Host

Consequences of immune
deficiency on HBV infection

Characteristics of Hepatitis B in immune deficiency
1. Immune suppression enhances viral replication.
2. Hepatitis B is more frequent in patients with immune suppression.
3. Lower rate of spontaneous recovery in acute cases.
4. Higher rate of chronic infection.
5. Higher frequency of HBe positivity.
6. Lower prevalence of anti-HBe seroconversion or HBs loss.
7. More rapid progression of fibrosis.
8. Higher risk of cirrhosis and HCC.
9. Higher morbidity and mortality.

 This harmful impact of immune deficiency on the natural history of chronic
HBV infection is related to the following factors:
1. High viral load enhances the progression of fibrosis per se, the risk of cirrhosis and
HCC.
2. Marked enhancement of viral replication may result in a rare severe liver disease,
called fibrosing cholestatic hepatitis, which is associated with the direct toxicity of
viral proteins.
3. Recognition of viral proteins expressed on the surface of infected hepatocytes by
the HBV-specific T cytotoxic lymphocytes results in hepatocyte destruction.
 Reduction or discontinuation of immune deficiency may result in severe
liver disease (eg, fulminant hepatitis) by immune restoration.

This trichrome stain of a case of fibrosing
cholestatic hepatitis

 Patients undergoing chemotherapy:
1. The risk of reactivation in HBsAg-positive patients undergoing chemotherapy is as
follows:
• Haematological malignancies: 33 to 67%
• Breast cancer: 41%
• Gastrointestinal cancers: 6.9%
1. This risk is independently increased in regimens that contain high doses of steroids,
rituximab or anthracyclines.
2. So, the degree of immunosupression may be more important than the underlying
malignancy.

4. Patient characteristics with an increased risk include:
• high serum HBV DNA prechemotherapy
• male sex
• high levels of ALT
5. Reactivation mortality rates have been reported to be between 5 and 40%.
6. More patients will develop jaundice, which may necessitate interruption of
chemotherapy and potentially lead to a poorer treatment outcome.

Immune deficiency
Chronic hepatitis
Fibrosing cholestatic
hepatitis
Extrahepatic impact
Acute
hepatitis
Fulminant
hepatitis
Discontinuation or delay of
specific therapies
Immune restoration Collateral damage

Treatment of Hepatitis B in immune deficiency
 Recommendations for treatment of hepatitis B carriers who require
immunosuppressive or cytotoxic therapy:
• HBsAg and anti-HBc: for patients who are at high risk of HBV infection. This is done
prior to treatment initiation.
• Prophylactic antiviral therapy is recommended for HBV carriers at the onset of cancer
chemotherapy:
1. If baseline HBV DNA <2,000 IU/mL: continue treatment for 6 months after
completion of chemotherapy or immunosuppressive therapy.
2. If baseline HBV DNA >2,000 IU/mL: continue treatment until the patient
reaches treatment endpoints as in immunocompetent patients.

Treatment of Hepatitis B in immune deficiency
 Recommendations for treatment of hepatitis B carriers who require
immunosuppressive or cytotoxic therapy:
3. Lamivudine or telbivudine can be used if:
• the anticipated duration of treatment is short (<12 months), and
• baseline serum HBV DNA is not detectable.
3. Tenofovir or entecavir is preferred if:
• longer duration of treatment is anticipated.
3. IFN- should beɑ avoided in view of the bone marrow suppressive effect.

Consequences of immune
deficiency on HCV infection

Characteristics of Hepatitis C in immune deficiency
 The relationship between HCV infection and immunosuppression is complex
and multifaceted.
 This ranges from enhancement to inhibition of HCV replication and from
worsening to improvement of liver damage.
 These different outcomes depend on:
• The type of immunosuppression.
• Baseline liver damage.
• Pathological condition to be treated.

 Despite the fact that hepatocytolysis occurs secondary to the attack by
cytotoxic T lymphocytes against the HCV-infected cells, the liver disease is
usually exacerbated and more rapidly evolutive in immunosuppressed
patients.
 The risk of developing rapidly evolving, difficult-to-control liver disease
appears to be lower than in the case of HBV infection.
 Less cautious approach is allowed if immunosuppressive therapy is
considered urgent and necessary.
 However, accurate screening and specialized advice is recommended as soon
as possible in HCV-positive patients.

Time to develop liver cirrhosis in immunocompetent and immunosuppressed
patients:
Category of Patients Median/range (years)
Immunocompetent 30/13-42
Hypogammaglobulinemia 8.8/4.5-15
HIV-HCV co-infection 10/6-30
Bone marrow transplantation 10.1/1.2-24.9
Liver transplantation 2/1-4

1. Cancer treatment may exacerbate the viral infection and lead to other complications,
such as liver failure or even death.
2. Immunosuppression following stem cell or bone marrow transplantation or
treatment with monoclonal antibodies such as rituximab can cause reactivation of
the virus (i.e., sharp increases in the serum ALT level and viral load).
3. Hepatotoxicity of some anticancer drug regimens should be taken in consideration.
4. Because cancer is usually the more immediate threat, its treatment typically takes
precedence in patients who also have HCV.
5. HCV treatment lasts 6–12 months; most of our patients do not want to delay cancer
treatment that long, or their cancer is one that needs to be treated immediately.

6. Many patients begin HCV treatment after the completion of chemotherapy or stem
cell transplantation.
7. However, HCV treatment is not always delayed. “If a patient with HCV and
hepatocellular carcinoma is recommended for a liver transplant, we begin HCV
treatment while the patient is on the transplant list to eradicate the virus before the
donor organ becomes available, thus preventing the infection of the new liver.
8. Immediate HCV treatment might also be recommended for a patient who needs
chemotherapy with hepatotoxic drugs that would cause liver failure unless the virus
is first eradicated.

9. A patient’s life expectancy may affect his or her decision to undergo HCV
treatment.
10. Quality of life issues also may affect patients’ decisions.
11. The HCV cure rate among cancer patients is 30%–40%, which is lower than that in
the general HCV patient population.
12. Try avoid concomitant HCV therapy and chemotherapy because interferon and
ribavirin are myelosuppressive.

Management of Viral Hepatitis in Immunocompromised Patients

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